This combined clinical and laboratory investigationi of danazol-treated patients with myelodysplasia examines the mechanism by which danazol exerts its beneficial effects in this disorder. Cytopenias in myelodysplasia have been attributed primarily to ineffective hematopoiesis by an abnormal clone in the bone marrow, which has a replicative advantage over normal marrow precursors, However, our initial studies suggest that immunologically-mediated accelerated peripheral destruction of blood cells contributes to the cytopenias, and that enhanced blood cell celarance is due to surface alterations of the cells produced by the abnormal clone. This study seeks to determine if danazol's effects in myelodysplasia are primarily due to inhibition of peripheral blood destruction or enhanced hematopoiesis. Ninety patients with myelodysplasia and symptomatic cytopenias will be accrued over 2 1/2 years. Before and after three and six months of danazol therapy, patients will be evaluated for response to treatment, and the following laboratory studies will be performed: quantitation of platelet-associated immunoglobulin and complement and of monocyte Fc (1gG) receptor number; marrow karyotyping; and growth patterns and karyotypes of marrow cultured in the presence of cis-retinoic acid, corticosteroid or danazol. Patient accrual will be adequate to allow correlation of danazol-induced clinical responses with presenting clinical and morphologic features, marrow culture results, cytogenetic analyses and immunologic abnormalities and with the changes that occur in these studies during danazol therapy. The results of this study will: expand our knowledge of danazol's mechanism of activity; identify which subsets of myelodysplasia, defined clinically, morphologically and biologically, respond to danazol therapy; enhance our knowledge of the interactions between immunoglobulins and cell surfaces; and provide new information about the nature and effects of the maturational abnormalities in myelodysplasia.